The Guanidine Bases in the Blood of Dogs with Experimental Hypertension Produced by Constriction of the Renal Arteries.

When Goldblatt and coworkers (1) in 1934 first announced that a significant and sustained elevation in arterial blood pressure could be produced in dogs by constriction of the renal arteries they also reported a few experiments in which the level of the guanidine bases in the blood stream of these animals had been followed. Although their preliminary studies indicated that these substances were not involved in either the production or maintenance of this type of experimental hypertension, they suggested that the results were not conclusive and that the group as a whole deserved further study. It is the purpose of this report to record the results of several experiments which have been undertaken in this laboratory in an effort to determine what relationship, if any, these bases bear to this type of hypertension. That there might be some relationship between the guanidine bases and hyperpiesia is not a particularly new concept. In 1924 Major and Stephenson (2) emphasized that many of these substances produced a marked and prolonged rise in blood pressure. Following Major's initial studies several efforts have been made to demonstrate an increased amount of the guanidine bases in the blood of hypertensive patients (3) as well as in eclampsia (4). That these investigations have been inconclusive is evidenced by the contradictory nature of the reports that have appeared up to the present time. Of further interest are the experiments of Minot and Dodd (5) who report that an accumulation of guanidine bases is present in the blood stream of dogs in which a ricin necrosis has been produced. Therefore, not only because of the normal existence of these substances and their excretion by the kidney, but also because of their relationship to degenerating tissue, it has seemed significant to establish what relationship, if any, they might bear to that type of experimental hypertension which may be produced by constriction of the renal artery.